I am an ME/CFS sufferer,
science graduate and medical science Masters student and would like to
submit some comments on your draft research strategy on ME/CFS.

I thought that the
draft was very thorough and of very high quality, so my comments are relatively
small points which may or may not be of use to you. I will list
them in the order in which the associated points were made in the draft.
You may well have already taken some or all of the matters into account,
of course, so please forgive my presumption..

Re initial summary
points 10 and 11: there is a need to distinguish factors which trigger
the development of the illness from factors which aggravate the condition
after it has developed. Although some factors may be involved in
both processes, others are probably only involved in one or the other.
There is potential for substantial symptomatic relief via the identification
and removal of aggravating factors, and this can probably be done relatively
easily via the scrutiny and collation of clinical records.

Re point 48:
because initial triggering factors may no longer be detectable after the
illness has developed, there is a need to take biological samples and
measurements at the earliest possible stage when patients present with
ME/CFS-like symptoms. In my own case I believed that a trigger was
organophosphate poisoning, but I did not have my plasma AChE tested until
long after the exposure. The other problem with this test is that
a baseline (pre-exposure) measurement is required in order to assess the
significance of post-exposure measurements. Perhaps it would be
possible for such measurement to be done on a routine basis in well people.
(Also see comments on points 113 & 117)

Re point 63:
there appears to be genetic susceptibility to Bell's Palsy (or possibly
another illness with similar consequences, such as a herpes infection)
in my family, so this may be a useful pointer, although I do not know
of any relatives with ME/CFS. I developed this paralysis at the
age of 5.

Point 76 refers to
some seriously affected patients never fully recovering (my underlining).
I am not seriously affected but have had the condition for 7 years, with
very gradual deterioration, so do not expect to recover. Thus I
do not believe that non-recovery necessarily correlates with severity.
Also see my comment re point 155.

Point 106 appears
to suggest that there is reduced motivation and responsiveness and appetite
and weight loss in ME/CFS sufferers. In my view this is over-generalising.
Many sufferers are very well-motivated (indeed many are high-fliers and
workaholics) before the illness develops and, although a period of depression
may be associated with these symptoms in the early stages, such symptoms
are by no means universal in later stages. My depression (probably
part-emotionally and part-physically-based) only lasted for about two
years, including the first year in which physical ME/CFS symptoms were
present, and has been absent for the past 6 years, during which time I
have been very highly motivated and with a hearty appetite. Perhaps
this apparently incorrect conclusion has arisen due to the inappropriate
use of animal studies. One must bear in mind that humans have very
different and additional motivational systems from other species, and
I believe that the 'sickness behaviour syndrome' (SBS) referred to may
relate to co-occurring depression rather than to ME/CFS. You cannot
ask a non-human animal whether it is feeling depressed. Pursuance
of such a red herring risks wasting resources, developing inappropriate
treatments and delaying more productive research.

Point 108 advocates
studying SBS further using 'chronic models'. I am strongly opposed
to using animal models for the reasons given above as well as for ethical
reasons.

Re points 112 &
113, from conclusions drawn from the precursors of, and progression of,
my own illness I believe that there is a strong likelihood that a sustained
over-release of cortisol (e.g. due to stress of some kind) may lead to
a pathological negative-feedback process, perhaps via a reduction in cortisol
receptors, culminating in a drastic and persistent reduction in cortisol
release, which may be a primary factor in CFS/ME aetiology.

If interpretation
of basal cortisol levels is problematic, is this partly due to not knowing
what a patient's levels were before developing ME/CFS? If so, perhaps
cortisol levels should be measured routinely (as recommended for AChE
in my comment re point 48).

Re point 117:
Biochemical tests for all patients presenting with possible early ME/CFS
symptoms might help here (as recommended in my comment re point 48).

Re point 120:
a district nurse told me that she had observed a generational alternation
between rheumatoid arthritis and irritable bowel syndrome. It may
be worth looking at such generational alternations in the case of ME/CFS.
My IBS manifested itself before the ME/CFS, and IBS or similar bowel dysfunctions
appear anecdotally to be relatively common in people with ME/CFS (from
my correspondence with other sufferers). My father had RA.

Re point 123:
I profoundly disagree with the idea of studying human diseases in animals
on both scientific and ethical grounds. As stated in your draft,
there is a huge mass of actual and potential information available on
human sufferers. Causing further suffering is totally unjustifiable.
See my first point re Annex 1.

Point 137 asks whether
depression is integral to, or a response to, CFS/ME. It also needs
to be considered whether depression can have a causal role (see my comment
on points 112-3 re cortisol).

Re point 155:
This suggests a correlation between severity and duration of illness.
I am not convinced of this as it does not seem to apply in my case (also
see my comment re point 76). Thus it is important to treat severity
and duration as separate variables.

I was somewhat dismayed
at the reference to 'competitiveness' in point 184. This is not
a competition - it is about human welfare. Information in medical
science should be shared at all stages, and collaboration should be maximal
both nationally and internationally. In case 'the need to attract
high-quality researchers' suggests that this must involve high monetary
rewards and 'perks', I do not believe that the best researchers require
a high income to motivate them. Financial inducements are more likely
to attract those whose motivations are non-altruistic. Scientific
discovery and advances in human well-being are their own rewards for the
right people.

Re Annex 1, I agree
strongly with the charity representative's statement submitted by Kate
Saffin, Annette Hacket and Adele Wright about the need to use the vast
body of information which already exists. This should be one of
the first steps undertaken in the quest to solve the mysteries of CFS/ME.
This is relevant to my comments on points 106, 108, 123 on animal experiments.

Re 'Gaps in research;
defining the research agenda; there appears to be no agreed starting point'
(also in Annex): the untapped resource which I refer to above would
help to identify such a starting point. Although it is likely to
be rife with artefact and subjectivity, the size of the resource may be
large enough to iron out many such confounding factors.

Re 'Obstacles' (also
in Annex): Physical and psychological causes appear to be treated
here as discrete and separate. However, it may be difficult or impossible
(or indeed counter-productive) to separate them; it may be that in combination
they lead to the crossing of a threshold of some kind of stress (adrenocortical?).
For example, psychological stress depresses the immune system, which can
then allow opportunistic infections and perhaps anthropogenic toxins to
further weaken physiological systems.

Another potential
obstacle I would add is possible conflicts of interest in funding bodies.
Companies which manufacture chemicals (including pharmaceuticals) may
be reluctant to support research or publish findings which implicate their
products as causative or exacerbating factors in the illness. They
may also be over-eager to seek drug-based solutions, notwithstanding the
fact that a substantial proportion (perhaps the majority) of sufferers
have very low tolerance to pharmaceutical drugs (as has been my own experience),
and may actually have their condition worsened by them (as I believe may
be the case for myself).

Appendix: 'Finding
the cause': May I suggest also looking at Candida, IBS and 'leaky
gut' (see my comment on point 120). Re candida, we appear to have
deliberately engineered, via both conventional breeding and genetic modification,
strains of yeast which are highly resistant to destruction for the production
of alcoholic drinks and bread. Could this indestructibility also
persist within the body?

Also in Appendix:
'What it does to the body; area examples' refers to 'looking across systems
and traditional boundaries.' I agree with this approach totally,
for aetiology as well as pathology, as I have stated above.

I hope that at least some of these comments are useful.
Yours sincerely,
Vivien Pomfrey